背景：研究發現吸菸所產生的自由基會對蛋白質、DNA及脂質造成氧化傷害，進而導致動脈硬化、心臟疾病及癌症，一些體外試驗研究顯示，抗氧化物會抑制自由基及改善因吸菸所導致的分子生物傷害。目的：探討總抗氧化能力及氧化傷害與勞工吸菸行為之相關性。方法：本研究對象為職場勞工，利用橫斷性研究(cross-sectional study)，將研究對象分為：(一)對照組，未予以吸菸衛教介入。(二)衛教介入組。(三)衛教介入加尼古丁貼片組。依衛教介入模式評估吸菸行為對體內總抗氧化能力及氧化傷害指標8-OHdG之影響。本研究採總抗氧化能力(Total antioxidant capacity, TAC)測定儀(Photochem)，分析體內的水溶性及脂溶性總抗氧化能力，以此作為氧化能力指標。氧化傷害指標採競爭型酵素結合免疫分析法(enzyme linked immunosorbent assay；ELISA)原理，使用ELISA kit (Japan Institute for the Control of Aging , Fukuroi , Shizuoka , Japan)，可偵測濃度為0.125~10 ng/ml來分析尿中8-OHdG濃度。結果：將衛教加貼片介入組合併衛教介入組整體來看，以GEE分析，發現不論 ACL-D濃度、ACW-D濃度、ACL-D加ACW-D濃度均隨衛教次數而有增加抗氧化能力，其中ACL-D濃度達顯著差異。而針對體內氧化傷害指標(8-OHdG)濃度是否與衛教介入有關，從結果來看亦有相似趨勢，即是；衛教加貼片介入組與衛教介入組均發現可減少氧化傷害。結論：從目前結果可初步判斷吸菸可能導致抗氧化能力降低與增加氧化傷害情形發生。

Background: Previous studies found that the free radicals caused by smoking might have oxidative damages to proteins, DNA and lipid, and lead to diseases such like arteriosclerosis, heart disease and cancers. Some in-vitro tests show that the anti-oxidants may inhibit the free
radicals and improve in molecular biological damage caused by smoking. Objective: The pur-pose of this study was to evaluate the inter-relationships between total antioxidant capacity, oxidative damage and smoking behaviours. Methods: This study is cross-sectional. Subjects
were separated into:(1) control group, with no health education intervention; (2) group with health education intervention; (3) group with health education intervention and nicotine patches. Through the model of health education intervention, we evaluated the influence of smoking behaviours to human body’s total antioxidant capacity and oxidative damage index 8-OHdG. This study used total antioxidant capacity (TAC) photochem to analyze the water-soluble and oil soluble total antioxidant capacity, it can be seen as an integrated parameter for cumulative function of plasma and body fluids as the antioxidant capacity index. The antioxidant capacity index based on principles of enzyme linked immunosorbent assay, (ELISA), by ELISA kit, it may detect the concentration of 0.125~10 ng/ml to analyze the concentration of 8-OHdG in
urine. Results: We found that regardless of concentrations of ACL-D, ACW-D, ACL-D plus ACW-D, they antioxidant capacity increase with the number of health education increases, and further, the concentration of ACL-D was significant different from the other two. While focusing on the in-vitro oxidative damage index(8-OHdG), there was a similar trend from results of whether the concentration relates to health education intervention, that is, the oxidative dam-age decrease in both the group with health education intervention and nicotine patches and group with health education intervention.
Conclusion: Based on these preliminary results, we concluded that smoking behaviours might cause the decreases of antioxidant capacity and increases of oxidative damages.